Relational Analysis of the Phenomenon of Early School Leaving: A Habitus Typology

Although there is an extensive body of literature on the causes and consequences of early school leaving (ESL), little is known of how early school leavers cope with their situation after having left the education system. This paper's main objective is to fill this research gap. At first we look at developments in the social positioning of early school leavers in Austria that show that their situation has deteriorated not only because of changes in the labour market (e.g. due to globalization) but also because of displacement processes that are influenced by habitus formation and capital endowment. Drawing on Bourdieu's concepts of habitus and capital, we explored the situation of young people who had left school early. We used a multi-perspective approach and conducted 123 narrative interviews which we analysed by grouping cases that demonstrated similar social practice and perception patterns generated by a set of socially learned dispositions. Thus we were able to reconstruct a habitus typology consisting of seven different types: the "ambitious", the "status-oriented", the "non-conformist", the "disoriented", the "resigned", the "escapist" and the "caring". How young people experience stigmatization is the common thread that runs through all seven habitus types

Stochastic modelling, Bayesian inference, and new in vivo measurements elucidate the debated mtDNA bottleneck mechanism

Dangerous damage to mitochondrial DNA (mtDNA) can be ameliorated during mammalian development through a highly debated mechanism called the mtDNA bottleneck. Uncertainty surrounding this process limits our ability to address inherited mtDNA diseases. We produce a new, physically motivated, generalisable theoretical model for mtDNA populations during development, allowing the first statistical comparison of proposed bottleneck mechanisms. Using approximate Bayesian computation and mouse data, we find most statistical support for a combination of binomial partitioning of mtDNAs at cell divisions and random mtDNA turnover, meaning that the debated exact magnitude of mtDNA copy number depletion is flexible. New experimental measurements from a wild-derived mtDNA pairing in mice confirm the theoretical predictions of this model. We analytically solve a mathematical description of this mechanism, computing probabilities of mtDNA disease onset, efficacy of clinical sampling strategies, and effects of potential dynamic interventions, thus developing a quantitative and experimentally-supported stochastic theory of the bottleneck.Comment: Main text: 14 pages, 5 figures; Supplement: 17 pages, 4 figures; Total: 31 pages, 9 figure

41Ca in tooth enamel. part I: A biological signature of neutron exposure in atomic bomb survivors

The detection of 41Ca atoms in tooth enamel using accelerator mass spectrometry is suggested as a method capable of reconstructing thermal neutron exposures from atomic bomb survivors in Hiroshima and Nagasaki. In general, 41Ca atoms are produced via thermal neutron capture by stable 40Ca. Thus any 41Ca atoms present in the tooth enamel of the survivors would be due to neutron exposure from both natural sources and radiation from the bomb. Tooth samples from five survivors in a control group with negligible neutron exposure were used to investigate the natural 41Ca content in tooth enamel, and 16 tooth samples from 13 survivors were used to estimate bomb-related neutron exposure. The results showed that the mean 41Ca/Ca isotope ratio was (0.17 ± 0.05) × 10-14 in the control samples and increased to 2 × 10-14 for survivors who were proximally exposed to the bomb. The 41Ca/Ca ratios showed an inverse correlation with distance from the hypocenter at the time of the bombing, similar to values that have been derived from theoretical free-in-air thermal-neutron transport calculations. Given that γ-ray doses were determined earlier for the same tooth samples by means of electron spin resonance (ESR, or electron paramagnetic resonance, EPR), these results can serve to validate neutron exposures that were calculated individually for the survivors but that had to incorporate a number of assumptions (e.g. shielding conditions for the survivors).Fil: Wallner, A.. Ludwig Maximilians Universitat; Alemania. Universitat Technical Zu Munich; Alemania. Universidad de Viena; AustriaFil: Ruhm, W.. Helmholtz Center Munich German Research Center For Environmental Health; Alemania. Ludwig Maximilians Universitat; AlemaniaFil: Rugel, G.. Ludwig Maximilians Universitat; Alemania. Universitat Technical Zu Munich; AlemaniaFil: Nakamura, N.. Radiation Effects Research Foundation; JapónFil: Arazi, Andres. Universitat Technical Zu Munich; Alemania. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Faestermann, T.. Universitat Technical Zu Munich; AlemaniaFil: Knie, K.. Universitat Technical Zu Munich; Alemania. Ludwig Maximilians Universitat; AlemaniaFil: Maier, H. J.. Ludwig Maximilians Universitat; AlemaniaFil: Korschinek, G.. Universitat Technical Zu Munich; Alemani

Four and a half LIM protein 1C (FHL1C)

Four-and-a-half LIM domain protein 1 isoform A (FHL1A) is predominantly expressed in skeletal and cardiac muscle. Mutations in the FHL1 gene are causative for several types of hereditary myopathies including X-linked myopathy with postural muscle atrophy (XMPMA). We here studied myoblasts from XMPMA patients. We found that functional FHL1A protein is completely absent in patient myoblasts. In parallel, expression of FHL1C is either unaffected or increased. Furthermore, a decreased proliferation rate of XMPMA myoblasts compared to controls was observed but an increased number of XMPMA myoblasts was found in the G(0)/G(1) phase. Furthermore, low expression of K(v1.5), a voltage-gated potassium channel known to alter myoblast proliferation during the G(1) phase and to control repolarization of action potential, was detected. In order to substantiate a possible relation between K(v1.5) and FHL1C, a pull-down assay was performed. A physical and direct interaction of both proteins was observed in vitro. In addition, confocal microscopy revealed substantial colocalization of FHL1C and K(v1.5) within atrial cells, supporting a possible interaction between both proteins in vivo. Two-electrode voltage clamp experiments demonstrated that coexpression of K(v1.5) with FHL1C in Xenopus laevis oocytes markedly reduced K(+) currents when compared to oocytes expressing K(v1.5) only. We here present the first evidence on a biological relevance of FHL1C

Quantitative Analysis of Candida Cell Wall Components by Flow Cytometrywith Triple-Fluorescence Staining

This work was supported by the European Commission within the FP7 Framework Programme [Fungitect-Grant No 602125]. We also thank Thomas Sauer, Vienna Biocenter Campus (VBC), Austria, for technical support at the FACS facility of the MFPL, Karl Kuchler, MFPL-Department of Medical Biochemistry, Medical University of Vienna, Max F. Perutz Laboratories, Campus Vienna Biocenter, Vienna, Austria and Ernst Thuer, Centre for Genomic Regulation, Barcelona, Spain, for advice on statistical approaches. Neil Gow acknowledges the support of the Wellcome Trust and the MRC Centre for Medical MycologyPeer reviewedPublisher PD

Changing care services and labour markets

Changes in the nature of funding, in the care sector, are influencing the development of a social care labour market. Migration plays a role in ensuring the provision of care workers in many European countries